Focal nodular hyperplasia after orthotopic liver transplantation

Abstract

Focal nodular hyperplasia (FNH) has been well characterized in native livers, but to our knowledge, no cases of FNH have been described in liver allografts. We review the clinicopathological features of 6 FNHs identified in 4 patients after orthotopic liver transplantation. There were 3 male patients and 1 female patient ranging in age from 2 to 63 years. The time from transplant to a diagnosis of FNH ranged from 15 to 118 months. Two patients presented with an incidental solitary liver nodule. One patient presented with 2 liver nodules, and the other patient initially presented with 1 liver nodule and was found to have another nodule at autopsy 6 years later. Two FNHs were seen as an incidental finding at autopsy, and the other 4 were initially identified on ultrasound. Follow-up magnetic resonance imaging and computed tomography scans revealed features atypical for FNH and suspicious for hepatocellular carcinoma. The initial diagnosis of FNH was made by needle core biopsy in 3 cases and at autopsy in 2 cases. The lesions ranged in size from 1.7 to 6.9 cm. Three patients had conditions associated with altered hepatic vascular perfusion; 2 patients had portal vein thrombosis, and 1 had a partial allograft from a living donor. In conclusion, FNH can present as a hepatic nodule after orthotopic liver transplantation and should not be confused with hepatocellular carcinoma. Because of altered hepatic circulation in the posttransplant liver, a diagnosis of FNH would not be unexpected. 1-8 Hepatocellular carcinoma may be recurrent or de novo in patients with the known risk factors for this condition, especially recurrent viral hepatitis. Nodular regenerative hyperplasia is believed to represent hyperplastic growth of hepatocytes in response to abnormalities of hepatic blood flow.Similarly, focal nodular hyperplasia (FNH) is also thought to arise as a hyperplastic response to vascular abnormalities. Because alterations of hepatic vascular perfusion are frequent after liver transplantation, it would not be surprising to encounter FNH in a transplanted liver. However, a review of the literature did not reveal any cases of FNH arising within a transplanted liver. We herein review 4 cases and discuss the clinicopathological findings. PATIENTS AND METHODSThe cases were retrieved from the surgical pathology files of the University of California Los Angeles Center for the Health Sciences. Clinical, radiological, and follow-up information were obtained from reviews of the medical records. The surgical specimens were fixed in 10% buffered formalin, and sections were routinely processed and embedded in paraffin. Serial 4-m-thick sections were prepared for routine hematoxylin and eosin staining and histochemical staining.

Endovascular closure of a portocaval shunt after left lobe liver transplantation using an amplatzer muscular ventricular septal occluder device

“…With the last, graft atrophy and dysfunction with hyperammonemia and hepatic encephalopathy have been reported 5, 6. In addition, focal nodular hyperplasia, a polyclonal hepatic response to a variety of circulatory abnormalities that recently was reported to develop de novo in a living donor graft,9 was prominent in our patient and joins the list of long‐term sequelae of small‐for‐size syndrome.…”

An inflammatory myofibroblastic tumor in the transplanted liver displaying quick wash-in and wash-out on contrast-enhanced ultrasound

“…Hepatic lesions in grafted livers usually represent recurrent malignancy, [ 16 ] metastasis, or focal nodule hyperplasia. [ 17 ] CEUS can generally be used to differentiate effectively among these. [ 14 ] Quick wash-in and wash-out on CEUS has been widely accepted as a classic characteristic of hepatocellular carcinoma (HCC).…”

Extended follow‐up of pediatric liver transplantation patients receiving once daily calcineurin inhibitor

“…The proposed mechanism of fibrosis development is due to abnormalities in the hepatic circulation following a technical variant graft. Specifically, blood vessel architecture does not develop in a manner to support normal liver architecture, thus leading to focal nodular hyperplasia and consequently fibrosis . The patient who developed progression of fibrosis by >1 stage received a partial graft.…”